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<p>Cardiovascular health is negatively impacted by arterial stiffening, which increases pulsatile load and elevates left ventricular workload. Aortic dilatation may compensate for the pulsatile overload resulting from arterial stiffening. Previous studies have shown a negative correlation between diabetes and aortic diameter, suggesting that diabetes may impair aortic dilatation and thereby compromise compensatory buffering capacity. This study aims to explore the relationship between diabetes, aortic diameter, and left ventricular hypertrophy. This retrospective study included 271 elderly patients stratified by diabetes status. Aortic and cardiac geometry was measured via echocardiography, and arterial stiffness was assessed using brachial-ankle pulse wave velocity (baPWV). Pulse pressure (PP) was used as an index of pulsatile load. Linear regression and mediation analyses were conducted to examine the associations among diabetes, aortic diameter, arterial stiffness, PP, and left ventricular mass index (LVMI). Diabetes, fasting blood glucose (FPG), and glycated hemoglobin (HbA1c) were independently associated with smaller aortic diameters (AoRi), with regression coefficients of − 0.984, − 0.275, and − 0.479, respectively. BaPWV was positively associated with AoRi (a = 0.942,<i> P</i> = 0.015), whereas AoRi was negatively correlated with PP (b =−  0.990, <i>P</i> &lt; 0.001). BaPWV had a direct positive effect on PP (c′ = 3.336, <i>P</i> = 0.024), which was counteracted by an indirect effect through AoRi (− 0.933, 95% CI − 2.133, − 0.028). Mediation analysis revealed that AoRi attenuated the effect of PP on LVMI (0.439, <i>P</i> &lt; 0.001 vs. 0.308, <i>P</i> = 0.007) and amplified the effect of diabetes on PP (3.903, <i>P</i> = 0.031 vs. 4.732, <i>P</i> = 0.010). In the chain-mediated effect model, diabetes had a significant total effect on LVMI (β = 5.025, <i>P</i> = 0.043). The diabetes → AoRi → PP → LVMI pathway demonstrated a significant indirect effect (0.230, 95% CI 0.013–0.592). Diabetes is associated with impaired aortic dilatation and increased left ventricular hypertrophy, potentially serving as a pathological mechanism driving progression of myocardial hypertrophy.</p>

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Diabetes mellitus exacerbates cardiovascular remodeling in elderly Chinese by affecting aortic diameter and pulsatile load

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月2日

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  • Yuqi Jiang,
  • Ziwei Zhao,
  • JunFeng Jiang,
  • Yanxia Lin,
  • Pengcheng Jiang,
  • Yimeng Niu,
  • Huanrui Zhang,
  • Wen Tian

摘要

Cardiovascular health is negatively impacted by arterial stiffening, which increases pulsatile load and elevates left ventricular workload. Aortic dilatation may compensate for the pulsatile overload resulting from arterial stiffening. Previous studies have shown a negative correlation between diabetes and aortic diameter, suggesting that diabetes may impair aortic dilatation and thereby compromise compensatory buffering capacity. This study aims to explore the relationship between diabetes, aortic diameter, and left ventricular hypertrophy. This retrospective study included 271 elderly patients stratified by diabetes status. Aortic and cardiac geometry was measured via echocardiography, and arterial stiffness was assessed using brachial-ankle pulse wave velocity (baPWV). Pulse pressure (PP) was used as an index of pulsatile load. Linear regression and mediation analyses were conducted to examine the associations among diabetes, aortic diameter, arterial stiffness, PP, and left ventricular mass index (LVMI). Diabetes, fasting blood glucose (FPG), and glycated hemoglobin (HbA1c) were independently associated with smaller aortic diameters (AoRi), with regression coefficients of − 0.984, − 0.275, and − 0.479, respectively. BaPWV was positively associated with AoRi (a = 0.942, P = 0.015), whereas AoRi was negatively correlated with PP (b =−  0.990, P < 0.001). BaPWV had a direct positive effect on PP (c′ = 3.336, P = 0.024), which was counteracted by an indirect effect through AoRi (− 0.933, 95% CI − 2.133, − 0.028). Mediation analysis revealed that AoRi attenuated the effect of PP on LVMI (0.439, P < 0.001 vs. 0.308, P = 0.007) and amplified the effect of diabetes on PP (3.903, P = 0.031 vs. 4.732, P = 0.010). In the chain-mediated effect model, diabetes had a significant total effect on LVMI (β = 5.025, P = 0.043). The diabetes → AoRi → PP → LVMI pathway demonstrated a significant indirect effect (0.230, 95% CI 0.013–0.592). Diabetes is associated with impaired aortic dilatation and increased left ventricular hypertrophy, potentially serving as a pathological mechanism driving progression of myocardial hypertrophy.